Search PubMed⌕ Search

Biomedical subjects

F Di Pede

Publications and source records attributed to F Di Pede.

At least 73 records · Page 4Linked to original sources
PubMed1985

Reference equations for the single-breath diffusing capacity. A cross-sectional analysis and effect of body size and age.

A longitudinal study was implemented in an unpolluted rural area of northern Italy (near Venice), before the start of the operation of a large oil-burning thermoelectric power plant, in order to investigate the effects of the future exposure to air pollution and to elucidate the natural history of obstructive airways diseases. During the first cross-sectional survey, a sample of the general population (n=3,300, 8 to 64 yr of age) performed several lung function tests, and information on risk factors and on the presence of respiratory symptoms were obtained by a standardized questionnaire. There were 712 subjects who were classified as normal on the basis of rigid criteria and who were able to perform satisfactorily a single-breath CO diffusing capacity (DLCOsb) test. The DLCOsb values showed an increase with height and age early in life and a later decrease with age. Two age groups were selected to determine an age at which DLCOsb stopped increasing and began to decline. Reference equations were computed (using age and height) in these 2 different age groups in each of the sexes. Similar equations were calculated for the total lung capacity derived from single-breath helium dilution measurements. The DLCOsb values in this study were higher than reported by other investigators. The method of selection of the study population, the strict criteria for normal, as well as technical, differences probably explain this finding. Reference equations for diffusing capacity corrected to lung volume (DL/VA) were computed only for adults (much greater than 20) in both sexes, because age and height coefficients in young subjects were insignificant.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

[Idiopathic ventricular tachycardia responsive to verapamil. Presentation of 3 cases and review of the literature].

Recently a unique clinical entity has been suggested in subjects without apparent heart disease presenting with recurrent ventricular tachycardia (VT) characterized by RBBB + LAH electrocardiographic pattern, relatively slow rate, induction by atrial stimulation, and interruption by verapamil. According to these characteristics, three cases (2 M and 1 F, aged 18, 33 and 66 years) are presented in this study. They have had palpitations from one to twenty years, but not syncopal episodes. During VT the cycle length ranged from 300 to 480 msec. VT was terminated both by verapamil and by ajmaline. VT was inducible in 3/3 cases by incremental atrial pacing when cycle length of pacing became similar to that of spontaneous VT; in 2/3 cases VT was induced by programmed right atrial stimulation and in 2/3 cases by programmed ventricular stimulation. Serial electrophysiological studies for pharmacological and therapeutic evaluation applied to 1/3 cases showed: amiodarone given orally (200 mg/die) for two months prevented the induction of VT while verapamil, propranolol, mexiletine, and propafenone tested intravenously were ineffective. In the remaining two patients amiodarone, tested only intravenously, was not effective to prevent the induction of VT but lengthened its cycle length. All patients received amiodarone orally (200 mg/die) and were followed for 2,7 and 8 years respectively. Two of them had no more episodes of VT and one, while asymptomatic, continued to present with. The electrophysiological mechanism of this form of VT cannot be identified with certainty, but many data suggest a reentry in the posterior fascicle of left bundle branch as the most probable mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

[Predictive value of the ajmaline test in dysfunction of the sinus node. Prospective 4-year follow-up relative to 77 patients].

To establish the usefulness of Ajmaline test for the evaluation of sinus node function, 77 pts (47 M, 30 F, mean age +/- SD = 61 +/- 15 yrs) first underwent an electrophysiologic study and then were followed-up for a mean period of 46.3 months. The following parameters were determined before and after i.v. administration of Ajmaline (1 mg/kg in 1 minute): sinus cycle length (SCL), corrected sinus node recovery time (CSNRT) and sino-atrial conduction time (SACT). The pts were divided into 3 groups: Group A: 10 pts without clinical or electrocardiographic signs of sinus node dysfunction (SND) and with normal control CSNRT and SACT (less than or equal to 500 and less than or equal to 120 msec, respectively); Group B: 46 pts with clinical-electrocardiographic signs of suspected or apparently not severe SND (sinus bradycardia greater than or equal to 40 beats/min and/or syncopes with positive vagal manoeuvres) and/or slightly abnormal control CSNRT (greater than 500 less than or equal to 600 msec) and/or SACT (greater than 120 less than or equal to 150 msec); Group C: 21 pts with clinical-electrocardiographic signs of apparently severe SND (sinus bradycardia less than or equal to 39 beats/min, sino-atrial block, sinus arrest) and/or definitely prolonged control CSNRT and/or SACT (greater than 600 and greater than 150 msec, respectively). The Ajmaline test was considered negative for the presence of a severe SND if SCL was not prolonged after the administration of the drug more than 20% and CSNRT and SACT were not prolonged more than 50% compared to the control values. Otherwise the Ajmaline test was considered positive. Twenty-seven out of the 77 pts studied underwent permanent pacemaker implantation (23 immediately after the electrophysiologic study and 4 during the follow-up). The following results were obtained: the Ajmaline test was negative in 100% of group A, 87% of group B and 48% of group C pts and positive in 0% of group A, 13% of group B and 52% of group C pts; during the follow-up a negative test resulted predictive in 56 out of 60 pts (92%) and a positive test in 16 out of 17 pts (94%). The predictive accuracy of the test was, therefore, 93.5%. These results indicate that Ajmaline test is an useful provocative test for disclosing, during electrophysiologic studies, pts who have severe SND and for selecting those who need pacemaker implantation.

Adolescent↗
PubMed1984

Value of serial electropharmacological testing in managing patients resuscitated from cardiac arrest.

Electrophysiologic studies were performed in 11 patients (9 men, 2 women; mean age: 59.9 yrs) who had survived an episode of cardiac arrest due to ventricular tachycardia (VT) or ventricular fibrillation. The purpose of the studies was to evaluate the usefulness of serial acute drug testing in selecting an effective chronic antiarrhythmic regimen. Ten of the patients were suffering from chronic ischemic heart disease with one or more previous myocardial infarctions while one had no evidence of structural heart disease. A ventricular aneurysm was present in four of them. During control electrophysiologic study, a sustained VT was induced by ventricular stimulation (single and double extrastimuli at various paced ventricular cycle lengths plus bursts of rapid ventricular pacing) in nine of the ten patients (90%) who were studied while not receiving antiarrhythmic drugs; a non-sustained VT was induced in one of them (10%). In three patients (30%) VT could be initiated only by right ventricular stimulation at a side different from the apex (outflow tract). No arrhythmia was observed in the only patient who was studied while taking amiodarone orally (400 mg/day for more than three months). During serial acute drug testing a totally effective drug regimen (successful in preventing the induction of any ventricular arrhythmia) was found in seven of the ten patients (70%) who underwent this procedure and a partially effective drug regimen (a sustained VT was no longer inducible; it was easier to interrupt and it was considerably slower) was found in two patients (20%). None of the nine patients who received chronic antiarrhythmic therapy based on the results of serial acute drug testing died suddenly during a mean follow-up of 14 months (range: 3-28) and only one had a recurrence of cardiac arrest. The latter, however, was taking antiarrhythmic drugs at a dosage less than that proved to be effective during electropharmacological testing. The only patient who refused serial acute drug testing and received an empiric antiarrhythmic therapy died suddenly at the 21st month of follow-up. These results indicate that serial electropharmacological testing is useful in selecting an effective long-term drug regimen in survivors of cardiac arrest.

Adrenergic beta-Antagonists↗
PubMed1984

[Intrinsic function of the sinus node in patients with syncope and positive vagal maneuvers].

This study was undertaken to establish the nature (intrinsic or extrinsic) of sinus node dysfunction in patients presenting with syncope and abnormal response (sinus pause greater than 3'') to vagal manoeuvres (carotid sinus massage and/or eye-ball compression). To this purpose 29 patients (20 males, 9 females, aged 18-79 yrs, mean = 60) underwent an electrophysiologic study. In all we measured before and after autonomic blockade with Propranolol (0.2 mg/kg) and Atropine sulfate (0.04 mg/kg) the following parameters: sinus rate, corrected sinus node recovery time and sino-atrial conduction time. According to the presence or absence of electrocardiographic signs of sinus node dysfunction the patients were divided into three groups: Group A: 11 patients without electrocardiographic signs of sinus node dysfunction; Group B: 13 patients with borderline electrocardiographic signs of sinus node dysfunction (sinus bradycardia between 40 and 60 beats/min); Group C: 5 patients with definite electrocardiographic signs of sinus node dysfunction (sinus bradycardia less than or equal to 39 beats/min and/or sinoatrial block and/or sinus arrest). Fifteen patients (52%) had signs of organic heart disease. The main results obtained were: At least one electrophysiological test (sinus rate, corrected sinus node recovery time or sino-atrial conduction time) was abnormal in 10 patients (34,5%) before autonomic blockade and in 8 patients (27%) after autonomic blockade. Two of these 8 patients belonged to Group A (18%), 1 to Group B (8%) and 5 to Group C (100%). Six of these 8 patients were suffering from an organic heart disease and 2 were not.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

[Value of a serial electropharmacologic study in survivors of a cardiac arrest secondary to ventricular tachycardia or ventricular fibrillation].

Electrophysiologic studies were performed in 10 patients (8 M, 2 F, mean age: 60.2 yrs) who had survived an episode of cardiac arrest due to ventricular tachycardia (VT) or ventricular fibrillation. The purpose was to evaluate the usefulness of serial acute drug testing in selecting an effective chronic antiarrhythmic regimen. The cardiac arrest had always been sudden and unexpected. It occurred outside the hospital in 7 cases and in the hospital in 3 cases. Patients in whom cardiac arrest was associated with evidence of acute myocardial infarction were excluded from the study. Nine of the patients were suffering from chronic ischemic heart disease with 1 or more previous myocardial infarctions while 1 had no evidence of organic heart disease. A ventricular aneurysm was present in 4 of them. During control electrophysiologic study a sustained VT was induced by ventricular stimulation (single and double extrastimuli at various paced ventricular cycle lengths + bursts of rapid ventricular pacing) in 9 of the 10 patients (90%) and a non sustained VT was induced in 1 of them (10%). In 3 patients (30%) VT could be initiated only by right ventricular stimulation at a site different from the apex (outflow tract). During serial acute drug testing a totally effective drug regimen (successful in preventing the induction of any ventricular arrhythmia) was found in 6 of the 9 patients (66.7%) who underwent this procedure and a partially effective drug regimen (sustained VT no longer inducible, easier to interrupt and considerably slower) was found in 2 patients (22.2%). None of the patients who received a chronic antiarrhythmic therapy based on the results of serial acute drug testing died suddenly during a mean follow-up of 14.8 months (range: 3-29) and only 1 had a recurrence of cardiac arrest. The latter, however, was taking antiarrhythmic drugs at a dosage less than that proved to be effective during electropharmacological testing. The only patient who refused serial acute drug testing and received an empiric antiarrhythmic therapy died suddenly at the 21st month of the follow-up. It is also noteworthy that amiodarone, alone or in combination, was given chronically to 6 of our patients (60%). These results 1) indicate that serial electropharmacological testing is useful in selecting an effective long-term drug regimen in survivors of cardiac arrest, and 2) suggest that amiodarone may be effective in preventing sudden death in these patients.

Adult↗
PubMed1984

Mid-diastolic intraventricular functional block. A new mechanism for intermittent intraventricular blocks?

Experimental and clinical studies have demonstrated the existence of phase 3 and phase 4 functional blocks. In this report six cases are presented in which the electrophysiological study demonstrated the existence of a functional intraventricular block different from phase 3 and phase 4 blocks. In these cases the occurrence of the block was related to the presence in mid-diastole of a zone of block preceded and followed by intervals of unimpaired conduction. In two of 6 cases the functional block (infrahisian block) was not present in the basal tracing; it occurred during programmed atrial stimulation in a range of critical H1H2 coupling intervals delivered late in diastole, and did not appear after earlier stimuli. In the remaining four cases the conduction disturbance (2 RBBB, 2 infrahisian blocks) was present in the basal tracing, but disappeared both during early and late supraventricular extrastimuli, the first having short H1H2 intervals, the latter having H1H2 intervals longer than H1H1 basal cycle length. The width of the mid-diastolic zone of block varied from a few msec to hundreds of sec, and increased as heart rate increased. Two hypotheses are put forward in order to explain the electrophysiological mechanism responsible for the phenomenon: 1) a longitudinal dissociation in the conducting system, generating two different ways, one having a long refractory period, the other having a phase 4 spontaneous depolarization; they would be responsible of phase 3 and phase 4 blocks respectively. The early and late zones of conduction could be explained by an alternate conduction in one of the two ways, while the mid-diastolic zone of block could be due to a simultaneous block in both ways; 2) the existence of a diastolic oscillatory potential (late after-depolarization). In the latter case we can suppose that the mid-diastolic block was due to the stimulation of the cells of the conducting system before the restoration of the normal diastolic potential. Our electrophysiological data offer a new contribution to the understanding of intermittent intraventricular blocks. However further experimental and clinical studies are needed to confirm our electrophysiological hypotheses.

Adult↗
PubMed1983

Possible role of a ventricular conduction disturbance in the electrogenesis of the ECG-VCG signs of myocardial infarction.

The typical QRS patterns of myocardial infarction (MI-QRS) are commonly attributed to myocardial cellular death. However, observation of a transient appearance of MI-QRS during coronary insufficiency, the disappearance of MI-QRS after coronary by-pass surgery and the appearance of MI-QRS after intracranial hemorrhage suggest that a different electrophysiological mechanism may be at work. There is a single convincing explanation for all these observations. It seems possible, at least theoretically, that a localized conduction disturbance can generate or contribute to the generation of the MI-QRS. The results obtained in nine out of 194 cases studied by means of premature right atrial stimulation (PRAS) in our laboratory seem to confirm this hypothesis. In five of them we observed typical MI-QRS in the aberrant beats which were absent in the basal tracings. In the other four cases, MI-QRS which were present in basal tracings disappeared in the aberrant beats. In three of these a reduction in the duration of QRS was also observed, while in the fourth the duration of QRS did not change. In no case could the alterations of QRS (induction or disappearance of MI-QRS) be explained by a classical conduction disturbance, preexcitation or by a premature ventricular beat. While the induction of MI-QRS was clearly due to an aberrant conduction in the supraventricular beats, the disappearance of basal MI-QRS changes in premature supraventricular beats is more difficult to explain. One possible electrophysiological mechanism could be a supernormal phase conduction. If this is the case, the basal MI-QRS could be due to a ventricular conduction disturbance. In conclusion, our results suggest that MI-QRS can be generated, at least in our cases, by a localized conduction disturbance.

Adult↗
PubMed1982

[Clinical significance of corrected sinus node recovery time and natural and unnatural history of sinus node dysfunctions. A four-year prospective follow-up of 101 cases].

The clinical significance of corrected sinus node recovery time (CSNRT) and the natural and unnatural history of sinus node dysfunctions are not completely known. To gain some insight into this problem, 101 patients (pts) (54M, 47F, mean age +/- SD = 62.02 yrs +/- 14.42) with clinical and ECG signs of definite or suspected sick sinus syndrome (SSS) underwent an electrophysiologic study and then were prospectively followed for a mean period of 44.36 months +/- 18.96 (range: 2-78 months). The pts were divided into two groups: 1) Group A: 68 pts with prolonged CSNRT (greater than 500 msec); 2) Group B: 33 pts with normal CSNRT. Thirty-three pts of Group A (48.5%) and 2 pts of Group B (6.1%) received VVI pacemaker implantation (PM) immediately after the electrophysiologic study. The following results were obtained: 1) Pts of Group A showed a higher prevalence of organic heart disease and of ECG signs of definite SSS than pts of Group B. (p less than 0.05). Moreover, the higher the CSNRT in Group A pts, the more severe the ECG abnormalities of SSS. 2) Pts without PM, both of Group A and Group B, noted during the follow-up period a disappearance of neurological symptoms (syncopes and/or dizziness) and of ECG abnormalities of SSS in more than 50% of the cases. However, this was less evident in Group A pts compared with Group B pts (53.8% vs 78.6% regarding neurological symptoms and 54.3% vs 74.1% regarding ECG abnormalities of SSS) as well as in pts with organic heart disease in comparison with those with primitive SSS. Moreover, the number of pts who needed PM implantation during the follow-up period due to the worsening of clinical and ECG signs of SSS were higher in Group A than in Group B (20% vs 6.5%). The occurrence of cardiac death among the pts without PM was similar in pts of Group A (8.5%) and in those of Group B (9.7%). One pt of Group A without PM died suddenly (less than 1 hour). 3) Pts who required PM implantation were older (p less than 0.01) and showed a prevalence of organic heart disease higher (p less than 0.05) than those who did not require PM implantation. Pts with PM, both of Group A and Group B, showed a complete disappearance of syncopes and a clear-cut reduction of dizziness after implantation of it. On the contrary, dyspnea nearly always persisted and sometimes appeared when initially absent. Sudden and non-sudden cardiac death in PM pts (13.6%) was somewhat more frequent than in those without PM. 4) The incidence of stable atrial fibrillation was 12.1% in pts without PM and 27.2% in pts with PM. The occurrence of stable atrial fibrillation in pts without PM was generally not followed by clinical improvement. 5) The incidence of cerebrovascular accidents was approximately 8%. The accidents always occurred in pts with organic heart disease and often in the older pts (mean age: 75.1 yrs +/- 5.7) particularly in those with PM. A bradycardia-tachycardia syndrome was observed only in 3 pts who had a stroke...

Cardiac Pacing, Artificial↗
PubMed1981

["Left bundle branch block" pattern induced by premature right atrial stimulation. Electrogenetic and clinical considerations (author's transl)].

Although in the last years very important knowledges have been obtained in the field of the intraventricular conduction disturbances, many electrocardiographic-vectorcardiographic findings concerning the left bundle branch block (LBBB) and their electrogenesis are still controversial. With the purpose to clarify this problem we have reviewed and analysed 23 cases in whom BCG-VCG patterns of "complete" or "incomplete" LBBB were induced by the premature right atrial stimulation (PRAS) during an electrophysiologic study in man. The analysis of these cases have demonstrated that: 1) the same LBBB pattern can be caused by a slowed conduction or block at different sites of left intraventricular conduction system i.e. not only in the main stem of the left bundle branch (LBB) (tronkular LBBB) but also within the bundle of His (intra-His LBBB) or in all the three fascicles of the LBB distally to its subdivision (divisional LBBB); 2) ECG-VCG are not able to distinguish the anatomical or functional site of slowed conduction or block; 3) the right or left axis deviation in the LBBB is not due to LBBB per se but it represents or a block at two different sites, i.e. a tronkular or intra His LBBB plus a block in the anterior or posterior subdivision of the LBB, or a block at only one side i.e. a tronkular, intra-His or divisional LBBB but with prevalent involvement of one fascicle of the LBB; 4) the ECG-VCG "incomplete" LBBB pattern is similar to that of the left ventricular enlargement; 5) figures of "atypical LBBB" are not specific of myocardial necrosis; 6) the criteria for the diagnosis of "complete" LBBB are not reliable. We conclude that, since LBBB pattern does not always correspond to a slowed conduction or block in the main stem of the LBB, the current terminology of LBBB is inappropriate and could be changed with another which considers the site of delayed activation and not the site of slowed conduction. Therefore we propose the following terminology: 1) generalized left ventricular activation delay instead of LBBB without axis deviation; 2) generalized left ventricular activation delay superiorly predominant instead of LBBB with left axis deviation; 3) generalized left ventricular activation delay inferiorly predominant instead of LBBB with right axis deviation.

Adult↗
PubMed1981

[The right ventricular activation in ventricular activation delays. An endocardial mapping study (author's transl)].

To investigate the right ventricular activation, filtered bipolar recordings (1 cm interelectrode distance) of Apex (RVA), Inflow tract (RVIT) and Outflow tract (RVOT) of the right ventricle were obtained in 4 groups of subjects. 1st group: 25 cases with normal QRS; 2nd group: 7 cases with left ventricular conduction disturbances (4 LBBB and 3 LAH patterns); 3rd group: 20 cases with chronic coronary heart disease (CCHD) and RBBB alone (5 cases) or combined with LAH (15 cases); 4th group: 9 young subjects without heart disease (7 cases) or ostium secundum atrial septal defect (2 cases) and RBBB pattern. The activation times were calculated from the beginning of the QRS in the first endocavitary rapid deflection. The data obtained (average +/- s.d.) for QRS duration (QRSd), RVA, RVIT and RVOT were respectively: 1st group: 97 +/- 9, 23 +/- 9, 36 +/- 9, 39 +/- 8; 2nd group: 133 +/- 43, 20 +/- 14, 25 +/- 9, 42 +/- 6; 3rd group: 152 +/- 12, 49 +/- 13, 61 +/- 18, 82 +/- 20; 4th group: 130 +/- 17, 39 +/- 12, 58 +/- 12, 55 +/- 27. Activation times as expected were similar in 1st and 2nd groups. Significant differences were noted between 1st and 3rd groups (p less than 0.001) in activation times of RVA, RVIT and RVOT. Between 1st and 4th group significant differences were noted in activation times of RVA and RVIT (p less than 0.001) while no significant differences were observed for RVOT (p greater than 0.05). In 2 cases of the third group (CCHD) and in the 2 cases of atrial septal defect the activation time of RVA was within the normal range suggesting a peripheral block. In the cases of the 3rd group with troncular RBBB activation times of RVIT and RVOT were significantly related to the QRSd (r = 0.79 and 0.65, p less than 0.001 and less than 0.01 respectively), while there was no significant correlation between the activation time of RVA and the QRSd. In accordance with other Authors our study demonstrates that: 1) the RBBB pattern in ASD has a peripheral electrogenesis; 2) the RBBB pattern in CCHD is generally due to a troncular block but our study also suggests the possibility of a distal block in these patients. In contrast with some Authors the RBBB pattern in young people without heart disease was due to a troncular and not to a peripheral block. Finally, the absence of correlation observed in the cases with troncular block of the 3rd group: 152 +/- 12, 49 +/- 13, 61 +/- 18, 82 +/- 20; 4th group: 130 +/- 17, 39 +/- 12, 58 +/- 12, 55 +/- 27. QRSd and RVIT and RVOT activation times might be explained as follows: 1) in high degree troncular block the RVA activation time is due to the time employed byt the wave front to cross the septum which is probably similar in all the cases; 2) the QRSd depends on the activation time of the peripheral areas which depends on the variable spread of activation of the right ventricle probably due to a variable participation of the specialized conduction system.

Adolescent↗